Arı Murat, Erdogan Mumin Alper, Erbaş Oytun
Söke Health Services Vocational School, Aydin Adnan Menderes University, Aydin, Turkey.
Faculty of Medicine, Department of Physiology, Izmir Katip Celebi University, Izmir, Turkey.
BMC Pharmacol Toxicol. 2025 Jan 22;26(1):15. doi: 10.1186/s40360-025-00849-8.
Diabetic neuropathy (DN) is a heterogeneous condition characterized by complex pathophysiological changes affecting both autonomic and somatic components of the nervous system. Inflammation and oxidative stress are recognized contributors to the pathogenesis of DN. This study aims to evaluate the therapeutic potential of dichloroacetic acid (DCA) in alleviating DN symptoms, focusing on its anti-inflammatory and antioxidant properties.
Thirty-two adult male Sprague Dawley rats were divided into four groups: Control, Diabetic, and two DCA-treated groups receiving 5 mg/kg and 10 mg/kg of DCA, respectively. Diabetes was induced with streptozotocin (STZ) injections. Assessments included lipid peroxidation levels, plasma fibroblast growth factor-21 (FGF-21) and transforming growth factor-beta (TGF-β) levels, electrophysiological measurements, histological examination of the sciatic nerve, and motor function tests.
Treatment with DCA significantly reduced malondialdehyde (MDA) levels, indicating decreased lipid peroxidation. Plasma TGF-β levels were also lower in the DCA-treated groups, suggesting diminished inflammation. Conversely, plasma FGF-21 levels were elevated. Electrophysiological assessments revealed enhanced compound muscle action potential (CMAP) amplitudes and reduced distal latencies in DCA-treated rats, indicative of improved nerve conduction. Histopathological examinations showed reduced perineural thickness in the sciatic nerves of DCA-treated rats, pointing to decreased fibrosis. Enhanced performance in motor function tests was observed in these rats, implying improved muscle strength and motor capacity.
The study demonstrates that DCA therapy significantly reduces oxidative stress and inflammation in a rat model of DN, thereby ameliorating neuropathic symptoms. These results support the potential of DCA as a promising therapeutic agent for DN treatment. Further research is warranted to explore its clinical applications and to provide more detailed insights.
糖尿病性神经病变（DN）是一种异质性疾病，其特征在于影响神经系统自主和躯体成分的复杂病理生理变化。炎症和氧化应激被认为是DN发病机制的促成因素。本研究旨在评估二氯乙酸（DCA）在减轻DN症状方面的治疗潜力，重点关注其抗炎和抗氧化特性。
将32只成年雄性Sprague Dawley大鼠分为四组：对照组、糖尿病组以及两个分别接受5mg/kg和10mg/kg DCA治疗 的组。通过注射链脲佐菌素（STZ）诱导糖尿病。评估包括脂质过氧化水平、血浆成纤维细胞生长因子-21（FGF-21）和转化生长因子-β（TGF-β）水平、电生理测量、坐骨神经组织学检查以及运动功能测试。
DCA治疗显著降低了丙二醛（MDA）水平，表明脂质过氧化减少。DCA治疗组的血浆TGF-β水平也较低，提示炎症减轻。相反，血浆FGF-21水平升高。电生理评估显示，DCA治疗的大鼠复合肌肉动作电位（CMAP）幅度增加，远端潜伏期缩短，表明神经传导改善。组织病理学检查显示，DCA治疗的大鼠坐骨神经神经周厚度减小，提示纤维化减轻。在这些大鼠中观察到运动功能测试表现增强，意味着肌肉力量和运动能力提高。
该研究表明，DCA治疗可显著降低DN大鼠模型中的氧化应激和炎症，从而改善神经病变症状。这些结果支持DCA作为一种有前景的DN治疗药物的潜力。有必要进行进一步研究以探索其临床应用并提供更详细的见解。
